Complete spinal transection is followed by a transient depression of reflexes caudal to the lesion ("spinal shock"). Reflex depression is maximal shortly after the transection and thereafter reflexes gradually increase toward normal and eventually may reach supranormal levels. Although post-transectional reflex alterations have been studied in experimental animals and humans using conventional reflex testing techniques, little information is available with respect to the changes at the individual neuronal level which underly the alterations. The objective of the proposed research is to determine those changes in the membrane properties of spinal motoneurons and/or in synaptic transmission in motoneurons which may account for the depression and subsequent recovery of reflex activity in the spinal monsynaptic pathway. For this purpose, motoneurons of lightly anesthetized cats will be impaled with intracellular micropipettes. The resting membrane potential, firing threshold and input impedance of individual montoneurons will be measured before and after surgical transection or after functional interruption of descending spinal tracts by local cooling of the spinal cord. In addition, by application of the quantum hypothesis of synaptic transmission to the spinal monosynaptic pathway, the amount of transmitter released from Group Ia afferent terminals will be determined before and after spinal transection. With these criteria, it will be possible to identify whether presynaptic and/or postsynaptic changes underly post-transectional alterations in transmission in the spinal monosynaptic reflex arc.